RETRACTED: PEDF prevents reactive oxygen species generation and retinal endothelial cell damage at high glucose levels

Banumathi, Elayappan; Sheikpranbabu, Sardarpasha; Haribalaganesh, Ravinarayanan; Gurunathan, Sangiliyandi

doi:10.1016/j.exer.2009.09.014

Cited by 24 publications

(19 citation statements)

References 41 publications

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“…PEDF is becoming widely recognized as an important determinant of oxidative stress (Zhang et al 2008, Banumathi et al 2010, inflammation and angiogenesis (Jenkins et al 2007, Zhang et al 2008, is inversely associated with insulin sensitivity and metabolic flexibility (Richards et al 2010), is positively associated with characteristics of the metabolic syndrome (Yamagishi et al 2006), and is predictive of future clinical events in patients with heart failure (Rychli et al 2010). Contrary to animal and cell culture data (Lashbrook & Steinle 2005, Steinle et al 2008, we have demonstrated that short-term inhibition of the sympathetic nervous system does not affect circulating concentrations of PEDF.…”

Section: Women Basalcontrasting

confidence: 44%

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Newsom

Richards²,

Johnson³

et al. 2010

Journal of Endocrinology

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Sedentary behavior is associated with an attenuated thermogenic response to b-adrenergic receptor (b-AR) stimulation, an important regulator of energy expenditure (EE) in humans. Chronic stimulation of b-ARs, via heightened activity of the sympathoadrenal system, leads to diminished b-AR function. We have investigated the hypothesis that the thermogenic response of sedentary adults to b-AR stimulation will be increased during short-term sympathoadrenal inhibition. Using a randomly ordered, repeated measures study design, resting EE (REE; indirect calorimetry, ventilated hood technique) and the % increase in EE above REE (%DEE) during acute i.v. isoproterenol administration (nonselective b-AR agonist; 6, 12, and 24 ng/kg fat-free mass per min) were determined in 16 sedentary adults (nine females and seven males, 25G1 years, body mass index: 26 . 1G0 . 9 kg/m 2 , maximal oxygen uptake: 40G2 ml/kg per min (meanGS.E.M.)) in the basal state and on the 6th day of transdermal clonidine administration (centrally acting a2-AR agonist; 0 . 2 mg/day).Relative to baseline, clonidine inhibited sympathoadrenal activity, as evidenced by decreased plasma norepinephrine concentration (1 . 04G0 . 13 vs 0 . 34G0 . 03 nmol/l; P!0 . 001), skeletal muscle sympathetic nerve activity (22 . 5G3 . 8 vs 8 . 5 G1 . 9 bursts/min; PZ0 . 003), and resting heart rate (63G2 vs 49G1 beats/min; P!0 . 001). Sympathoadrenal inhibition decreased REE (6510G243 vs 5857G218 kJ/day; P!0 . 001), increased respiratory exchange ratio (0 . 84G0 . 01 vs 0 . 86 G0 . 01; PZ0 . 03), and augmented the thermogenic response to b-AR stimulation (%DEE: 11G2, 16G2, and 24G2 vs 14G1, 20G2, and 31G2; PZ0 . 04). These data demonstrate that in sedentary humans, short-term inhibition of sympathoadrenal activity increases the thermogenic response to b-AR stimulation, an important determinant of EE and hence energy balance.

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Section: Women Basalcontrasting

confidence: 44%

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Newsom

Richards²,

Johnson³

et al. 2010

Journal of Endocrinology

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“…45 In recent years, accumulating evidence has suggested that PEDF protects retinal neurons from light-induced damage, oxidative stress, and glutamate excitotoxicity. 26,30,31,46,47 Results in recent reports also suggest that PEDF can act as an antioxidative agent to ameliorate some pathologic changes in DR. [31][32][33] Previous studies have shown that PEDF is involved in the pathogenesis of DR by regulating cytokine secretion in Müller cells, including VEGF, tumor necrosis factor (TNF)-␣, and PEDF itself. 36 -28 It is proposed that PEDF plays an important role in regulating the function of GLAST in Müller cells, by acting as an antioxidative agent.…”

Section: Discussionmentioning

confidence: 94%

“…Consequently, ROS production was selected as a measure of oxidative stress. [31][32][33] High glucose increased the levels of ROS in Müller cells, but the effects were inhibited by PEDF. GPx activity decreased when induced by high glucose; however, this effect was counteracted by PEDF treatment, at least partially.…”

Section: Discussionmentioning

confidence: 99%

“…Pigment epithelium-derived factor (PEDF) is a multifunctional protein that has been demonstrated as a major antiangiogenic factor, a neuroprotective agent, an anti-inflammatory factor, and an antioxidative agent in the eye. 26 -30 Banumathi et al 31 showed that PEDF has an antioxidant effect in bovine retinal endothelial cells at a high glucose level that could induce oxidative stress in several retinal cells including Müller cells. 26,27,31 Previous reports have suggested that PEDF mitigates inflammation and oxidative stress in retinal pericytes exposed to oxidized low-density lipoprotein involved in DR 32 and PEDF inhibits oxidative stress-induced apoptosis and dys-function of cultured retinal pericytes.…”

mentioning

confidence: 99%

“…26 -30 Banumathi et al 31 showed that PEDF has an antioxidant effect in bovine retinal endothelial cells at a high glucose level that could induce oxidative stress in several retinal cells including Müller cells. 26,27,31 Previous reports have suggested that PEDF mitigates inflammation and oxidative stress in retinal pericytes exposed to oxidized low-density lipoprotein involved in DR 32 and PEDF inhibits oxidative stress-induced apoptosis and dys-function of cultured retinal pericytes. 33 A recent report demonstrated that PEDF could be a therapeutic option for ameliorating the effects of advanced glycation end products and oxidative stress in DR. 30 Whether PEDF acts as an antioxidant agent to inhibit oxidative stress-induced dysfunction of GLAST in Müller cells remains unconfirmed.…”

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confidence: 99%

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Effect of Pigment Epithelium–Derived Factor on Glutamate Uptake in Retinal Müller Cells under High-Glucose Conditions

Xie

Qin

Cheng

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.A predominant function of Müller cells is to regulate glutamate levels, but it is compromised in diabetic retinopathy (DR). The present study was performed to determine the role of pigment epithelium-derived factor (PEDF) in glutamate uptake in retinal Müller cells in high-glucose conditions. METHODS. The levels of Kir4.1, PEDF, and GLAST in retinal Müller cells in high-glucose conditions were analyzed by Western blot analysis and real-time RT-PCR, and a glutamate uptake assay was undertaken to investigate the activity of GLAST. Intracellular reactive oxygen species (ROS) generation was measured, and a glutathione peroxidase (GPx) activity assay was performed to determine oxidative stress in the presence of high glucose. After being treated with PEDF in high-glucose conditions, these proteins (Kir4.1 and GLAST) and their mRNAs, glutamate uptake activity, and oxidative stress in Müller cells were investigated. A PEDF siRNA method was used to confirm the effect of PEDF on glutamate uptake activity in Müller cells. RESULTS. In high-glucose conditions, glutamate uptake and Kir4.1, PEDF, and GLAST expression in Müller cells decreased significantly. Simultaneously, ROS generation increased, and GPx activity decreased. PEDF treatment inhibited the highglucose-induced decreases in glutamate uptake and in Kir4.1 and GLAST expression and ameliorated oxidative stress. Moreover, downregulation of PEDF expression by siRNA in Müller cells resulted in decreases in glutamate uptake, Kir4.1 and GLAST expression, and induced oxidative stress. CONCLUSIONS. These findings suggest that PEDF acts as an antioxidative agent against the decrease in Kir4.1 and GLAST expression and compromise of glutamate uptake activity in

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Pigment epithelium‐derived factor delays cellular senescence of human mesenchymal stem cells in vitro by reducing oxidative stress

Cao

Yang

2013

Cell Biology International

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Mesenchymal stem cells (MSCs) are multipotent progenitor cells that represent a promising approach in the field of regenerative medicine; however, this potential diminishes with senescence. Pigment epithelium-derived factor (PEDF) gives some protection by reducing oxidative stress, which is known to accelerate cellular senescence. Thus we hypothesized that PEDF could delay senescence during MSC expansion by reducing oxidative stress. Proliferation and differentiation potentials, oxidative stress, senescence and p53/p16 expressions have been examined. In MSCs cultured under normoxic conditions treated with PEDF, proliferative lifespan in vitro was significantly increased compared with control group not given PEDF, with ∼10 additional population doublings (PD) occurring before terminal growth arrest. Most of the MSCs cultured under normoxic conditions ceased to proliferate after 20-28 PD, while few senescent cells were found in the hypoxic, PEDF-hypoxic and PEDF-normoxic cultures; this was associated with downregulation of p53 and p16 expression and decreased oxidative stress. PEDF also preserved differentiation potentials of MSCs compared with the control group. Thus PEDF suppression of oxidative stress delays cellular senescence and allows greater expansion of MSCs.

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RETRACTED: PEDF prevents reactive oxygen species generation and retinal endothelial cell damage at high glucose levels

Cited by 24 publications

References 41 publications

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Short-term sympathoadrenal inhibition augments the thermogenic response to β-adrenergic receptor stimulation

Effect of Pigment Epithelium–Derived Factor on Glutamate Uptake in Retinal Müller Cells under High-Glucose Conditions

Pigment epithelium‐derived factor delays cellular senescence of human mesenchymal stem cells in vitro by reducing oxidative stress

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